An infected Andersson lesion presented with incomplete paraplegia in a patient with ankylosing spondylitis. A unique case report with literature review

Introduction A relatively rare and unknown entity in patients with ankylosing spondylitis is the Andersson lesion (AL). It was first described by Andersson in 1937 as destructive vertebral or disco-vertebral lesion of the spine without history of trauma. AL may result from inflammation or stress fracture of the rigid spine, while there is no evidence for an infectious origin. To our knowledge, only one case with an infected AL has been published many years ago; we hereby present the second case, but the first one with severe neurologic deterioration. Case presentation A 79-year-old male patient was presented to our emergency department and his neurological examination on admission revealed incomplete paraplegia below the Th10 level. Plain radiograms at the level of 10th thoracic vertebra revealed a lesion mimicking a severe vertebral fracture. The computed tomography confirmed the diagnosis of the AL and due to the significant local instability and the neurologic deficit, the patient underwent posterior decompression and stabilization. During decompression, we noticed purulence and extensive debridement was performed. The cultures of the Th10 pus revealed Enterococus sp, while the same pathogen was developed to urine cultures. The patient received intravenous antibiotics for 4 weeks, followed by per os antibiotic therapy. At the 18-month follow-up our patient had significant improvement of this functional status. Discussion Most studies support that inflammatory or traumatic/mechanical (pseudarthrosis) etiology are the most possible causes of Anderson lesions. Possible neurological deterioration should be investigated and demonstrates significant spinal instability. The integrity of the posterior column should be investigated, and exclusion of other concomitant lesions should be done. In cases with instability due to the fractured posterior elements, surgical intervention is mandatory. Spine surgeons should be competent to differentiate fracture from the Andersson lesion. In this rare case we highlight also that spine surgeons should obtain intraoperative cultures in cases with Andersson lesions, to exclude the minor possibility of the infectious origin of the entity and/or the possible secondary contamination of the affected area.